Today we're wrapping up our series with Cyrus Khambatta! Thank you Cyrus!
Day 5: Eating
for Diabetes: The Truth About Controlling Blood Glucose
There is a lot of confusion about what diets are best for
diabetics. In today’s lesson, I’ll share
with you 6 principles about eating for diabetes that are backed by scientific
research, and have been shown in human studies to reverse the effects of
insulin resistance.
To Fat or Not to Fat?
That is the Question
The biggest debate in the nutrition world in our generation
is whether eating a low fat diet or high fat diet is better for you. Over 20 years ago, a low fat diet was
considered the healthiest diet, because high fat foods were thought to elevate
cholesterol and triglyceride levels in the blood, contributing to heart
disease. In the 1990’s along came Dr.
Atkins, who argued that fat was not the enemy, an instead vilified
carbohydrates. He reasoned that excess
carbohydrates are converted to fat and stored as fat, contributing to
conditions like obesity and type 2 diabetes.
In today’s nutrition world, the paleo diet has taken center stage. Proponents of this diet argue that eating
similarly to our ancestors – a high intake of unprocessed foods and a complete
elimination of refined products - is the most evolutionary accurate diet for humans,
and is the diet that is best suited for the inner workings of our digestive
systems.
It seems like every 10 years or so, a new breed of dietary
tribalism takes hold, changing public opinion on the “healthiest” diet for
human consumption. More importantly, the
opinion about whether fat is “healthy” or “unhealthy” changes about once a
decade. So what’s the answer? Is fat good or is fat bad? As a diabetic, should you be eating fat or
not eating fat? Should you be eating
carbohydrates or not eating carbohydrates?
Let’s go back to what we talked about on day 2. We said that excess fat has a nasty way of
being stored everywhere in your body. It
is stored inside of your muscle tissue.
It is stored in your liver. It is
stored in your heart. It is stored in
fat tissue. It is stored in your
pancreas. It is stored in your
intestine.
Excess fat is stored in all tissues in the human
body, including those that are not designed to store fat.
Ectopic Fat
Accumulation
Take a look at this picture.
This is a highly magnified view of a fatty liver that has accumulated
excess fatty acids over time. The fatty
acids are stained in purple, and are located in droplets within liver
cells. The fact of the matter is that
these purple droplets are not supposed to be as large or as numerous as they
are. This fatty liver is suffering from ectopic fat accumulation, a term that
means “the storage of fat in tissues that are not designed to store fat.”
We also learned on day 2 that excess fat storage impairs the
action of insulin. In simpler words:
The accumulation of fat in tissues that are not designed to store fat
sets the stage for insulin resistance.
So what causes ectopic
fat accumulation? Will eating fat
cause this problem? Will eating too many
carbohydrates cause this problem? What
about large amounts of protein, will that cause insulin resistance?
Glucose and Fat: The
Battle for World Domination
Fatty acids, glucose and protein (amino acids) all compete
for entry into body tissues. Fatty acids
and glucose are either burned for energy immediately, or stored and burned for
energy later. Protein is also burned for
energy, although amino acids (the building blocks of protein) are often
distributed around the cell to be used as part of the cellular
infrastructure.
When fatty acids and glucose are both present in the
bloodstream following a meal, they seek entrance into cells all throughout the
body. In an ideal world, both glucose
and fatty acids would be vacuumed and used equally. But in reality, glucose and fatty acids
compete with each other for entry into cells, and one of the two wins. Every time.
Can you guess which one?
Fatty acids win.
Fatty acids win because they can gain entry into the cell
faster than glucose. And guess what that
means? It means that glucose stays in
the bloodstream instead of being vacuumed into cells like we want. And when glucose stays in the bloodstream,
high blood sugar ensues.
The truth of the matter is that even a small amount of fat
can have a large effect on blood sugar control.
It only takes a small serving of fat to outcompete glucose, gaining
entry into tissues faster.
On average, a
meal containing 100 grams of carbohydrate and 0 grams of fat can be cleared
from the bloodstream in 3 hours in an insulin sensitive individual. The same meal containing 100 grams of
carbohydrate, when eaten together with 15 grams of fat may take up to 8 hours
to clear from the bloodstream. The
presence of only 15 grams of fat results in high blood sugar lasting up to 5
hours longer than normal.
Your mission as a diabetic health machine is to give
glucose a fighting chance. Allow glucose
the ability to enter body tissues by removing fatty acids - the one obstacle in
it’s path.
Glucose is Your
Body’s Preferred Fuel Source
Make no mistake, every tissue in your body is designed to
run on glucose. Unfortunately, we have
been told many times over that carbohydrates are the enemy. We have been told that carbohydrates turn to
fat. We have been told that
carbohydrates make you overweight.
We must make a distinction between REAL and FAKE
carbohydrates.
What are FAKE
Carbohydrates?
FAKE carbohydrates are foods that are high in carbohydrate
yet low in nutrients. FAKE carbohydrates
are the products of a manufacturing process.
FAKE carbohydrates often have additives, in order to replace the
nutrients that were lost through processing.
FAKE carbohydrates have a long list of ingredients, most of which are
hard to pronounce.
FAKE carbohydrates have names like High Fructose Corn Syrup
(HFCS), sugar, cane sugar, organic cane sugar, molasses, aspartame, splenda,
etc.
FAKE carbohydrates increase insulin resistance mainly
by increasing the amount of fat stored in the liver and abdomen1–4.
Refined (FAKE) carbohydrates
are found everywhere in the grocery store.
FAKE
carbohydrates are generally packaged, bottled, coated with sprinkles and
contain a long list of difficult-to-pronounce ingredients. As a general rule, if you don’t think that
your great great grandmother would recognize the food, it’s probably not
something you want to be putting into your body. Foods that were sold only a hundred years ago
were less refined, resulting in a higher consumption of perishable, REAL
food.
What are REAL
Carbohydrates?
REAL carbohydrates come in the form of fruits and vegetables,
and are generally perishable. They are
foods that you would find if you were walking through in nature, and foods that
require little to no preparation. They
contain a combination of complex and simple sugars, and are designed to taste
sweet and break apart into glucose molecules for use by all major tissues in
your body.
REAL carbohydrates are
fruits, vegetables, leafy greens, and legumes.
REAL
carbohydrates tend to have a short shelf-life because they are generally fresh
fruits and vegetables, containing a large quantity of water, fiber, vitamins,
minerals and antioxidants.
If you still need more convincing, take a look at the
references below. This is only a short
list of scientific articles that explain the effect of fatty acids on insulin
action. They contain a bit of technical
jargon, but explain how insulin resistance can be minimized simply by reducing
fat intake5–13.
Hungry for More? Read These References
1. Stanhope, K. L. et al.
Consumption of Fructose and High Fructose Corn Syrup Increase Postprandial
Triglycerides, LDL-Cholesterol, and Apolipoprotein-B in Young Men and Women. J.
Clin. Endocrinol. Metab. 96, E1596–E1605 (2011).
2. Stanhope, K. L., Schwarz, J.-M.
& Havel, P. J. Adverse metabolic effects of dietary fructose: results from
the recent epidemiological, clinical, and mechanistic studies. Curr. Opin.
Lipidol. 24, 198–206 (2013).
3. Stanhope, K. L. et al.
Consuming fructose-sweetened, not glucose-sweetened, beverages increases
visceral adiposity and lipids and decreases insulin sensitivity in
overweight/obese humans. J. Clin. Invest. 119, 1322–1334 (2009).
4. Goran, M. I. et al. The
obesogenic effect of high fructose exposure during early development. Nat.
Rev. Endocrinol. (2013). doi:10.1038/nrendo.2013.108
5. Delarue, J. & Magnan, C. Free
fatty acids and insulin resistance. Curr. Opin. Clin. Nutr. Metab. Care 10,
142–148 (2007).
6. Wang, P.-Y., Kaneko, T., Wang, Y.,
Tawata, M. & Sato, A. Impairment of Glucose Tolerance in Normal Adults
Following a Lowered Carbohydrate Intake. Tohoku J. Exp. Med. 189,
59–70 (1999).
7. Xiao, C., Giacca, A., Carpentier, A.
& Lewis, G. F. Differential effects of monounsaturated, polyunsaturated and
saturated fat ingestion on glucose-stimulated insulin secretion, sensitivity
and clearance in overweight and obese, non-diabetic humans. Diabetologia
49, 1371–1379 (2006).
8. Wolpert, H. A., Atakov-Castillo, A.,
Smith, S. A. & Steil, G. M. Dietary Fat Acutely Increases Glucose
Concentrations and Insulin Requirements in Patients With Type 1 Diabetes
Implications for carbohydrate-based bolus dose calculation and intensive
diabetes management. Dia Care 36, 810–816 (2013).
9. Pańkowska, E., Błazik, M. &
Groele, L. Does the fat-protein meal increase postprandial glucose level in
type 1 diabetes patients on insulin pump: the conclusion of a randomized study.
Diabetes Technol. Ther. 14, 16–22 (2012).
10. Gormsen, L. C., Nielsen, C., Jessen,
N., Jørgensen, J. O. L. & Møller, N. Time-course effects of physiological
free fatty acid surges on insulin sensitivity in humans. Acta Physiol. Oxf.
Engl. 201, 349–356 (2011).
11. Boden, G. Fatty acid-induced inflammation
and insulin resistance in skeletal muscle and liver. Curr. Diab. Rep. 6,
177–181 (2006).
12. Hession, M., Rolland, C., Kulkarni,
U., Wise, A. & Broom, J. Systematic review of randomized controlled trials
of low-carbohydrate vs. low-fat/low-calorie diets in the management of obesity
and its comorbidities. Obes. Rev. 10, 36–50 (2009).
13. Rosenfalck, A. M., Almdal, T.,
Viggers, L., Madsbad, S. & Hilsted, J. A low-fat diet improves peripheral
insulin sensitivity in patients with Type 1 diabetes. Diabet. Med. J. Br.
Diabet. Assoc. 23, 384–392 (2006).





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